Fortunately, the emergency crew recognised the problem and tried to clear the airway. There was no improvement so the Heimlich manoeuvre was performed and a large bone was expelled with immediate relief of the man’s respiratory distress. He was taken to A&E for assessment but discharged after 2 hours.

Remember

The Heimlich manoeuvre is used to expel an inhaled foreign body:

• Stand behind the patient

• Encircle the upper part of the abdomen, just below the patient’s rib cage, with your arms

• Give a sharp, forceful squeeze, forcing the diaphragm sharply into the thorax.

This should expel sufficient air from the lungs to force the foreign body out of the trachea. If this fails, urgent assessment by experienced ENT or cardiothoracic clinician is required. Fibre optic or rigid bronchoscopy will be required if obstruction beyond vocal cords.

Other causes of upper airway obstruction are shown in Table 11.1, all of which require emergency management, which is also shown.

Table 11.1 Causes of upper airways obstruction (with management strategies)

Cough

Cough is common and when persistent can cause considerable fear and distress. Apart from the immediate discomfort of coughing, paroxysmal cough can interrupt sleep, provoke retching or vomiting and, if severe, result in rib fractures or syncope. Always enquire about sputum and its colour.

Case history

A 67-year-old man is admitted to hospital with a myocardial infarct. Following successful coronary intervention he is discharged on anti-platelet therapy, atorvastatin and enalapril. When seen again 2 weeks later, he was very well but complained of a persistent hacking cough. This had been keeping him awake at night.

In this case, as the patient has only a cough and is not breathless, the cause is very likely to be the ACE inhibitor (enalapril). This should be stopped and an ACE receptor antagonist, e.g. vasartan started. Unlike ACE inhibitors, angiotensin receptor antagonists do not affect bradykinin metabolism and do not produce a cough.

Cough is provoked by stimulation of mucosal and stretch receptors of the lung. Accordingly it has a number of causes:

Investigations

All patients with persistent cough should have a CXR

Other investigations will depend on the likely cause, e.g. serial peak flow in asthma, contrast studies if gastro-oesophageal reflux or aspiration is suspected and sputum culture, including request for Mycobacterium tuberculosis isolation if the cough is productive.

Breathlessness and wheeze

Asthma causes breathlessness, cough and wheeze. However, all that wheezes is not asthma.

Information

• Asthma provocation tests might be required to exclude mild–moderate and variable bronchial irritability

• Bronchoscopy will be required in all chronic cases remaining undiagnosed

Differential diagnosis of asthma:

• COPD:

• Patient usually > 40 years of age

• Heavy smoker > 20 pack years. (Note: patients with asthma might also smoke)

• History of variable wheeze: in patients with asthma, chest wheeze is usually worse at night and may only be episodic.

• Upper airway obstruction with stridor:

• Occurs when there is a mechanical obstruction in the larynx or trachea

• Is heard during inspiration and expiration; but inspiratory sound when mouth open is most typical

• Might be associated with vigorous accessory muscle activity and obvious distress.

• Left ventricular failure (LVF):

• Acute LVF can be difficult to differentiate from asthma

• Nocturnal symptoms common to both.

Figure 11.1 shows causes and triggers of asthma.

Figure 11.1 Causes and triggers of asthma. RSV, respiratory syncytial virus; NSAIDs, non-steroidal anti-inflammatory drugs.

Information

Causes of stridor:

• Tumour

• Foreign body

• Bilateral vocal cord palsy

• Laryngeal oedema

• Thyroid goitre

Case history

A 24-year-old female was admitted to MAU with breathlessness for 6 h. She has had a ‘cold’ for 2 days. Past history revealed her being ‘chesty’ as a child. It was noticed that she could not complete sentences easily. Heart rate was 126/min and respiratory rate was 30/min. There was expiratory wheeze over the lung fields. This patient has severe acute asthma.

Remember

Severe acute asthma:

• Increased breathlessness/cannot complete sentences

• Respiratory rate > 25/min

• Heart rate > 100/min

• PEFR 30–50% of best

• Arterial oxygen saturation (SaO₂) < 92%

How would you manage this patient in A&E?

Immediate management should be:

• Reassurance that treatment will be effective

• Oxygen 40–60% (Keep SaO₂ > 90%)

• Nebulised short acting β₂ agonist (SAB), e.g. salbutamol 5 mg or terbutaline 10 mg) with oxygen. (NB only 10% of drug reaches the lungs)

• Systemic corticosteroids:

• Prednisolone 30–40 mg daily or

• IV hydrocortisone 200 mg 8-hourly

• Monitor SaO₂ by oximetry

• Arterial blood gases (ABGs):

• Initially if SaO₂ < 90%

• Re-check (2-hourly) if PaO₂ < 8 or PaCO₂ > 5 kPa until the PaCO₂ is stable and the saturation is >90%

• PEFR 4-hourly. Note: performing PEFR might be distressing for patient: do not demand unnecessary repeat testing

• ECG

• Chest X-ray.

30 min later there has been no significant improvement in her breathlessness and PEFR. What would you do next?

• Call for senior help.

• Continue with nebulised β₂ agonist, now with added ipratropium (500 µg). Repeat every 30 min if necessary.

• Intravenous aminophylline infusion can be used if patient does not respond to repeated nebulisation with β₂ agonist and ipratropium. However, do not use this if oral aminophylline has been taken.

Information

IV aminophylline:

• Ensure patient is not on oral theophylline (do not give aminophylline if patient is on oral aminophylline)

• Monitor BP and heart rate

• Loading dose 250–500 mg over 1 h

Infusion:

• 1 mg/kg over 4 h

• 0.5 mg/kg/h thereafter

• Check aminophylline level at 6–8 h after the start of infusion and adjust dose

Other therapy

• Intravenous β₂ agonist, e.g. salbutamol 3–20 µg/min is an alternative in most cases.

• Magnesium sulphate 1.2–2 g IV infusion over 20 min with cardiac monitoring.

Remember

Life-threatening acute asthma

• Silent chest, feeble respiration, cyanosis

• Bradycardia/hypotension, arrhythmia

• Exhaustion/confusion

• PEFR < 33% of best

• Arterial oxygen saturation < 92%.

Indications for HDU or intensive care

Presence of life-threatening features and:

• PaO₂ < 8 on 60% oxygen

• PaCO₂ >6 kPa

• Previous history of requiring ventilation.

Remember

• Beware of the SILENT CHEST!

If asthma is very severe, air entry will be minimal and breath sounds quiet or absent.

There is now improvement in PEFR and breathlessness with nebulised β₂ agonist and ipratropium. What treatment should be offered to her now?

Continuing management should be:

• Keeping SaO₂ > 90% with oxygen supplementation

• Corticosteroids: prednisolone 20–40 mg daily, on a reducing dose

• 2–4-hourly nebulised short acting β₂ agonist (SABA) therapy.

When could she be discharged?

The patient can be discharged when:

• Symptoms, particularly nocturnal symptoms, have improved

• Ideally, PEFR should be 75% of best and diurnal variation (i.e. ‘morning dips’) < 25%. If patient is improving and compliance expected to be good, an earlier discharge is reasonable.

24–48 h before discharge

• Add inhaled corticosteroids, e.g. beclometasone, to oral steroids.

• Replace nebulised bronchodilators with inhalers.

• Introduce long-acting inhaled β2 agonists, e.g. salmeterol.

• Check inhaler technique (? might need spacer).

• Determine the cause of this attack (non-compliance, infection, allergen exposure).

Talk to asthma nurse

At discharge, patient should have:

• Oral and inhaled corticosteroids and long acting inhaled β₂ agonist (LABA). SABAs can be used on an ‘as required’ basis.

• Peak flow meter and diary.

• Management plan if condition deteriorates.

Progress.

This patient was discharged after 7 days on treatment as above. She requires close follow-up because of the severe acute attack.

Discharge letter to GP should include:

• Admission and discharge PEFR

• Recommended GP follow-up in 1 week

• Asthma clinic follow-up, preferably within 4 weeks.

Hyperventilation

Case history

A 15-year-old schoolgirl is brought by her teacher to the A&E department with dizziness and feeling faint. You notice that she is anxious, sighing and has erratic ventilation. There are no other physical signs on examination. Her teacher volunteered that the girl was anxious about impending examinations.

What should you do?

Full examination, CXR, PEFR or spirometry, and arterial blood gases (even if oximetry is normal).

You have decided that her symptoms are due to hyperventilation. This should be confirmed by demonstration of a respiratory alkalosis with a low PaCO₂ and [H⁺] in the arterial blood. Reassure the patient and ask her to breathe into a closed paper bag: when settled she can be discharged with further reassurance. Note: mild asthma is a common provocative cause and might require further investigation.

Hyperventilation syndrome refers to a condition of recurrent attacks of anxiety, sometimes phobic in nature, and provoking such profound hyperventilation to cause a reduction in arterial pCO₂ that tetany occurs. Other features include perioral and digital paraesthesia, carpopedal spasm, muscle weakness, dizziness and a sense of impending loss of consciousness or fear.

An attack of hyperventilation can be induced by a strong emotional experience in otherwise normal individuals, e.g. witnessing an accident.

In many patients, the label of hyperventilation syndrome is inappropriately given when mild asthma or other conditions, such as heart failure, lie behind the respiratory sensation. Indeed, hypocapnia resulting from hyperventilation might further provoke bronchoconstriction.

Clinically obvious hyperventilation can also result from a metabolic acidosis and will be recognised by arterial blood gas analysis: a reduced pH and bicarbonate contrary to the alkalosis of respiratory hyperventilation.

Tetany: see p. 451; overbreathing can cause tetany (p. 451).

Progress.

This patient settled quickly. She was reassured that there was nothing seriously wrong with her. She was taken home to her parents with a pamphlet explaining the hyperventilation syndrome.

Haemoptysis

Case history

A 63-year-old male smoker presents with a 4-month history of cough. Recently he has been coughing up blood in his sputum. He has also been breathless on exertion.

Coughing up blood is a dramatic symptom and can be frightening to patients and their families.

Colour of blood – this can differ with different causes

• Pink frothy sputum: pulmonary oedema.

• Rusty sputum: pneumonia.

• Make sure it is not haematemesis, which would be suggested by:

• History of retching

• Altered blood (resembling coffee grounds)

• Low pH of contents.

Enquire about epistaxis, which may cause confusion. Blood-stained saliva suggests bleeding from gums.

Common conditions presenting with haemoptysis

• Carcinoma of the bronchus:

• Smoker

• Age > 40 years

• Usually abnormal chest X-ray.

• Pulmonary embolism:

• Risk factors for DVT

• Chest X-ray often negative

• History of acute breathlessness.

• Pulmonary tuberculosis:

• More common in Asian people (in the UK), people drinking alcohol in excess, patients with HIV infection

• Age often < 40 years

• Chest X-ray usually shows patchy opacities in the upper lobes.

• Bronchiectasis:

• History of purulent sputum and/or possibly recurrent haemoptysis over years

• Cystic lesions on chest X-ray at lung bases in some but not all patients

• High-resolution CT scan of the lungs is diagnostic, with bronchial dilation, loss of airway tapering at the periphery, bronchial wall thickening and thickening and cysts at the end of the bronchioles

• Bronchiectasis is also a feature of cystic fibrosis.

Remember

• Chest X-ray might be normal, e.g. pulmonary embolism

• Large opacity: consider malignancy or tuberculosis.

Less common causes of haemoptysis are:

• Vasculitis (both the following are ANCA positive):

• Granulomatosis with polyangiitis (Wegener’s)

• Microscopic vasculitis.

• Pulmonary haemorrhage:

• Goodpasture’s syndrome

• Idiopathic pulmonary haemosiderosis.

• Chronic venous congestion of lungs:

• Mitral stenosis

• Left ventricular failure.

• Aspergilloma: seen in association with cavitatory lung disease.

Management of this case

A chest X-ray was taken (Fig. 11.2 and Information box) which showed a pleural effusion and a hilar mass. The pleural effusion was aspirated and sent for cytology. A pleural biopsy was taken under ultrasound control and showed no evidence of malignancy on histology.

Figure 11.2 Chest X-ray showing a left pleural effusion and a hilar mass.

Video-assisted thoracoscopy was then performed and this allowed visualisation of the pleura. A biopsy taken showed a squamous cell carcinoma.

The patient was referred to the multidisciplinary team for discussion of treatment options.

Information

Chest X-rays

A standard chest X-ray (CXR) is taken posteroanteriorly (PA), with the patient facing the X-ray plate; the beam is directed at the patient’s back at a standard distance.

An emergency department film is often taken anteroposteriorly (AP), with the patient lying down (supine) on the X-ray plate; the beam is directed at the patient’s front – the distance from X-ray source can vary.

In an AP:

• Heart size and mediastinum are magnified.

• Pleural effusion which lies along back of chest cavity when patient supine might be missed.

• Film quality may be poor.

Don’t request an AP ‘portable’ film unless it would be unsafe for the patient to have a PA film.

Management of massive haemoptysis

As little as 250 mL can fill the bronchial tree and be life threatening. Happily, this is uncommon but nevertheless frightening for everyone involved:

• Monitor: oxygen saturation with oximetry, blood pressure and pulse rate.

• Perform CXR. Exclude coagulation defects.

• Endotracheal intubation and suction might be required.

• Urgent bronchoscopy by an experienced doctor is sometimes required.

• A cuffed tube can be employed to protect the unaffected lung. It is inserted into the bronchus via a bronchoscope.

• Bronchial artery embolisation is highly effective if the bleeding vessel can be identified.

Information

Massive haemoptysis can occur in the following conditions:

• Tuberculosis

• Bronchiectasis

• Aspergilloma

• Carcinoma of the bronchus

Remember

Only a minority of patients have a malignant cause of massive haemoptysis.

Chest pain

Diagnosing the cause of a chest pain is often difficult; it can be straightforward or take days to diagnose correctly. A careful history (eliciting site, character and radiation of the pain) is often more useful than tests:

• Exercise-induced central chest pain is usually cardiac in origin.

• Rest pain might be: cardiac, pleuritic, musculoskeletal, nerve root irritation, oesophageal, mediastinal or referred pain from abdomen.

• Lung diseases only cause pain if the pleura, mediastinum, intercostal nerves or bones are involved.

Is it pleurisy?

Sharp pain in the sides of the chest, which ‘catches’ with breathing. This is often accompanied by fever, cough ± sputum or haemoptysis, indicating underlying lung disease.

Think of:

• Pneumonia and pleurisy

• Pulmonary infarction/embolism

• Pneumothorax

• Malignant invasion of pleura.

Is it musculoskeletal?

• Trauma:

• Rib fracture: ‘point’ tenderness

• Crushed vertebra: pain often referred around the chest.

• Chronic pain:

• Osteoarthritis (OA): long history with acute episodes. Look for spinal deformity

• Rib or spine disease: might be metastatic cancer; local tenderness and swelling, lumps, history of cancer.

• Muscles: Bornholm’s disease. Follows an upper respiratory tract infection; a low-grade fever can occur. Ache in muscles. Might be tender. Definite cases rare.

• Costochondral junction: Tietze’s disease; local pain on pressure over junctions. Responds to NSAIDs.

Is it nerve root irritation?

• Typically in a dermatome distribution around the chest. Might be unilateral.

• Vertebral OA, osteomyelitis, prolapsed disc.

• Malignant nerve root compression.

• Herpes zoster (shingles): is there a vesicular rash? (pain may precede rash).

Is it oesophageal?

Reflux causes retrosternal burning pain, usually after food. Worse lying flat and eased by antacid. Can be severe and mimic myocardial infarction.

Oesophageal rupture

Central pain with shock. Might have associated pleural effusion. Occurs after severe vomiting or more commonly endoscopy at which dilatation has been performed for a malignant lesion.

Is it referred pain from outside the chest?

Diaphragm irritation may cause shoulder tip pain. Localisation might be difficult for the patient. Several abdominal emergencies might have chest pain with or without abdominal pain.

Think of:

• Acute cholecystitis

• Acute duodenal ulceration

Is it genuine?

Yes – nearly always. Exclude organic disease in all cases.

A tiny minority might be attention seeking or have psychiatric disease. Even patients with Munchausen’s syndrome might have genuine disease.

What tests do you need to do for chest pain?

After a good history and examination do (as a minimum):

• ECG – repeat if first ECG normal

• CXR

• Serum cardiac markers

• Full blood count, including ESR and CRP.

Many diagnoses will now be obvious but remember:

• A normal ECG does not exclude cardiac pain.

• A normal CXR does not exclude pulmonary embolism.

If still in doubt:

• Retake the history, re-examine the patient and consider unusual causes

• Is WBC or ESR raised?

• Is the patient pyrexial?

• Arrange further investigations, e.g. CT, MR scan.

Respiratory failure

Respiratory failure (PaO₂ < 8 kPa) is a common medical emergency often presenting with non-specific symptoms such as mild confusion or agitation. Recognition requires arterial blood gas (ABG) analysis (see below). Oximeters that estimate arterial oxygen saturation from the finger or ear lobe are useful in assessment or monitoring.

Oximeters might be falsely reassuring in the patient breathing oxygen. Importantly, they will not detect alveolar hypoventilation, producing high pCO₂.

Remember

All breathless patients should have oximetry checked at triage in A&E.

Respiratory failure commonly results from either a problem with the respiratory pump or because of intrinsic lung disease.

Remember

All unconscious patients should have ABG analysis at initial assessment.

With respiratory pump failure the arterial pCO₂ (PaCO₂) is raised. You should think of:

• Severe air-flow limitation, e.g. COPD

• Neurological depression, e.g. coma, sedatives, overdose

• Chest wall problem, e.g. flail chest, pneumothorax

• Neuromuscular disease, e.g. Guillain–Barré, old poliomyelitis.

In intrinsic lung disease (apart from COPD) hypoxaemia is often combined with a reduced PaCO₂

The hypoxaemia arises primarily from a mismatch of ventilation and perfusion in the pulmonary alveolar bed. Hypoxic stimulation of ventilation, coupled with abnormal respiratory sensation, then leads to a reduced arterial pCO₂ (alveolar hyperventilation). A raised PaCO₂ indicates impending respiratory arrest as it suggests either a reduction in ventilatory effort or failure of the respiratory pump.

In hypoxaemia with reduced PaCO₂ consider

• Infection, e.g. pneumonia

• Shock, e.g. sepsis, hypovolaemia, acute lung injury

• Asthma

• Cardiac disease, e.g. LVF, pulmonary hypertension

• Pulmonary embolism.

In respiratory failure arterial blood gas sampling is necessary to

• Assess severity

• Identify type, i.e. alveolar hypo- or hyperventilation

• Appreciate the degree of compensation (i.e. the chronicity of the condition)

• A coexisting metabolic acidosis commonly causes confusion and can be recognised by the base excess value (see below).

Information

ABG sampling is painful. Contrary to common belief, the use of local anaesthetic does not make the procedure more difficult. Heparin has a low pH and should be expelled from the syringe. Heparin-bonded microsamplers are available and small-diameter needles make local anaesthetic unnecessary. When taking ABG samples it is essential to note the inspiratory O₂ concentration (FiO₂).

Summary of acid–base changes (Fig. 11.3)

In a respiratory acidosis

Carbon dioxide clearance is reduced – there is alveolar hypoventilation. The PaCO₂ and [H⁺] rise. The HCO₃ is also increased due to renal compensation.

Figure 11.3 The Flenley acid–base nomogram. The bands show the 95% confidence limits representing the individual varieties of acid–base disturbance. The central white box shows the approximate limits of arterial pH and pCO₂ in normal individuals.

Examples: exacerbation of COPD, flail chest injury, Guillain–Barré syndrome.

In a respiratory alkalosis

There is alveolar hyperventilation and both the PaCO₂ and [H⁺] are decreased. The HCO₃ is slightly decreased. Examples: acute asthma, anxiety attack.

In a metabolic acidosis

There is disturbance of bicarbonate regulation or excessive H⁺ production. The HCO₃ is reduced and the PaCO₂ falls because of respiratory compensation.

Example: diabetic ketoacidosis, renal failure, shock.

In a metabolic alkalosis

The HCO₃ is increased and relative hypoventilation leads to a small compensatory increase in the PaCO₂.

Example: excessive vomiting, profound hypokalaemia.

Normal blood gas values (with F_iO₂ 21%):

• pH ~ 7.4

• PaO₂ > 10.0 kPa *

• PaCO₂ 4.5–6.0 kPa †

• HCO₃ 24–28 mmol/L.

Information

The base excess value provided by the ABG analyser is calculated by back titration to normal values for PaCO₂ and HCO₃.

Common ABG abnormalities

Life-threatening asthma

Supplemental O₂ is being provided (note the high PaO₂). There is a metabolic acidosis (note the pH and BE) as a result of metabolic demands exceeding O₂ delivery and producing a lactic acidosis. Airflow limitation limits the normal respiratory compensation to this profound acidosis.

Acute or chronic respiratory failure in a patient with COPD

Acute or chronic respiratory acidosis exacerbated by a high F_iO₂ using variable performance mask (40–60% O₂) (note high PaO₂ and PaCO₂). The high HCO₃ results from renal compensation. The patient was changed to 28% oxygen.

Severe pneumonia (F_iO₂ 60%)

Despite high F_iO₂ this patient is hypoxaemic because of ventilation: perfusion mismatch. The profound hypoxia despite oxygen and the associated metabolic acidosis indicate the need for urgent intubation and IPPV and are a reflection of circulatory failure resulting from septic shock.